摘要
The experimental model of traumatic brain injury was established in Sprague-Dawley rats according to Feeney’s free falling method.The brains were harvested at 2,6 and 24 hours,and at 3 and 5days after injury.Changes in brain water content were determined using the wet and dry weights.Our results showed that water content of tissue significantly increased after traumatic brain injury,and reached minimum at 24 hours.Hematoxylin-eosin staining revealed pathological impairment of brain tissue at each time point after injury,particularly at 3 days,with nerve cell edema,degeneration,and necrosis observed,and the apoptotic rate significantly increased.Immunohistochemistry and western blot analysis revealed that the expression of occludin at the injured site gradually decreased as injury time advanced and reached a minimum at 3 days after injury;the expression of connexin 43 gradually increased as injury time advanced and reached a peak at 24 hours after injury.The experimental findings indicate that changes in occludin and connexin 43 expression were consistent with the development of brain edema,and may reflect the pathogenesis of brain injury.
The experimental model of traumatic brain injury was established in Sprague-Dawley rats according to Feeney＇s free falling method. The brains were harvested at 2, 6 and 24 hours, and at 3 and 5 days after injury. Changes in brain water content were determined using the wet and dry weights. Our results showed that water content of tissue significantly increased after traumatic brain injury, and reached minimum at 24 hours. Hematoxylin-eosin staining revealed pathological impairment of brain tissue at each time point after injury, particularly at 3 days, with nerve cell edema, degenera- tion, and necrosis observed, and the apoptotic rate significantly increased. Immunohistochemistry and western blot analysis revealed that the expression of occludin at the injured site gradually de- creased as injury time advanced and reached a minimum at 3 days after injury; the expression of connexin 43 gradually increased as injury time advanced and reached a peak at 24 hours after in-jury. The experimental findings indicate that changes in occludin and connexin 43 expression were consistent with the development of brain edema, and may reflect the pathogenesis of brain injury.
基金
supported by the Natural Science Foundation of Guangdong Province,No.10151600101000002
关键词
创伤性脑损伤
连接蛋白
发病机制
脑水肿
免疫印迹分析
SD大鼠
病理损伤
神经细胞
neural regeneration
traumatic brain injury
brain edema
connexin 43
occludin
nerve cells
pa-thology
tight junction
grants-supported paper
neuroregeneration
